Clinical cardiac electrophysiology techniques and interpretations pdf

  1. Clinical Cardiac Electrophysiology: Techniques and Interpretations.
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Clinical Cardiac Electrophysiology Techniques And Interpretations Pdf

This book covers all the important aspects of cardiac electrophysiology, pre- Clinical Cardiac Electrophysiology: Techniques and Interpretation, 4th Edition. Clinical Cardiac Electrophysiology Fellowship Teaching Objectives for the the basic science, clinical com- heart disease and VT developed the technique of . cardiology fellow for ECG interpretation as outlined by the American College of. skills expected of the certified clinical cardiac electrophysiologist in the broad domain of Ordering and interpreting results of tests . Implantation techniques.

In this issue of the Methodist DeBakey Cardiovascular Journal, we focus on new developments in cardiac electrophysiology. As is true for any field in medicine, cardiac electrophysiology EP continues to evolve, but its changes have been particularly dramatic over the past few years. Clinical EP came of age in the s as a diagnostic discipline devoted to the understanding and interpretation of intracardiac electrograms and their responses to pacing maneuvers. In the early s, a true revolution began with the advent of catheter ablation technologies, most saliently radiofrequency ablation, which rapidly became the standard of care for supraventricular and ventricular arrhythmias. Despite these advances, atrial fibrillation AF remained a tremendous challenge—not only because our understanding of its mechanisms lagged behind that of other arrhythmias but also because of the magnitude of the health care problem it represented. Atrial fibrillation affects millions of people in the United States and is a major cause of stroke, disability, dementia, and mortality.

The rate of diastolic depolarization in the SN is affected by both sympathetic adrenergic and parasympathetic muscarinic stimulation. This is predominantly affected by the If channel. Sympathetic adrenergic stimulation results in an increase in the gradient and duration of diastolic depolarization with minimal effects on the overall action poten- tial duration [8].

This occurs as a result of a shift in the activation curve to more positive voltages without a change in the conductance of the If channel as a result of an increase in intracellular cAMP [9]. The reverse occurs with parasympathetic muscarinic stimulation [10]. The delayed rectifier Ik channel is the predominant potassium channel in the SN and contributes to repolarization allowing the following depolarization to be initiated.

Respiratory sinus arrhythmia occurs as a result of a reduction in the PP inter- val with inspiration and a prolongation of the PP interval with expiration. The maxi- mum difference between the longest PP and shortest PP interval should be less than ms.

This phenomenon reduces with age. SN dysfunction encompasses sinus bradycardia, sinus pause, sinoatrial exit block, chronotropic incompetence and inappropriate sinus tachycardia. Sinus bradycardia is a relatively common finding and in the absence of symp- toms is generally of no clinical significance. A sinus pause is defined as the absence of a P wave for greater than or equal to 2 s although generally not considered clini- cally significant unless greater than or equal to 3 s while awake or 5 s while asleep.

If the duration of the sinus pause is a multiple of the PP interval, then sinoatrial node exit block should be considered. Inappropriate sinus tachycardia is a persistent elevation in heart rate greater than bpm at rest with no obvious precipitating cause.

There is an exaggerated increase in sinus rate with minimal activity and a reduction or normalization of sinus rate during sleep. The p wave morphology and axis are unchanged. It is important to rule out all potential causes as well as other arrhythmias such as right atrial tachycardia close to the SN or SN re-entry tachycardia.

Pharmacological options for inappropriate sinus tachycardia include beta adrener- gic blockers, nondihydropyridine calcium channel blockers and the selective If channel inhibitor ivabradine. Given the selective nature of ivabradine this has been shown to have a useful role in patients with symptomatic inappropriate sinus tachy- cardia unresponsive to beta adrenergic blockers and calcium channel blockers [12].

Further data is awaited whether this may be considered as first line treatment in this condition. Catheter ablation for SN modification is an alternative strategy in select cases of inappropriate sinus tachycardia.

The SN is often difficult to modify from the RA endocardium as there are multiple connections with sites of early activation between the SN and the RA. Additionally the bulk of the SN is subepicardial, has a signifi- cant amount of connective tissue, is often covered by thick muscle of the CT and there is a significant cooling effect from the SN artery.

Although acute results are good long term maintenance is less successful [14]. High output pacing should be performed at sites being considered for ablation to avoid phrenic nerve injury. The need for a permanent pacemaker is unusual but a potential com- plication of this procedure. The pectinate muscles which form the right atrial appendage span out from the CT.

Approximately two thirds of focal atrial arrhythmias occur along this structure [16]. RA Conduction Following discharge from the SN, conduction occurs through the RA using the mus- cular architecture of the atrial wall that comprises muscle bundles with well aligned working myocytes that preferentially carry the sinus impulse [17]. The notion of three specific internodal tracts is controversial because histologically specialized tissue tracts akin to the insulated ventricular conduction bundles have never been demonstrated anatomically.

Instead, it is a muscle bundle with well aligned myocytes, superfi- cially located across the anterior interatrial groove. Its rightward extension reaches superiorly to the area of the sinus node and inferiorly toward the right atial vesti- bule. Usually it is the most prominent interatrial bundle [18]. Conduction in this region is slow due to the criss-cross arrange- ment of the myocytes and distal ramifications of the crista terminalis relative to the better aligned and circumferential arrangement of myocytes in the vestibule leading to the tricuspid valve TV [19].

In the RAO position the catheter is moved from the right to the left keeping the catheter inferiorly. The EV separates the vestibular Fig. The Eustachian ridge is an elevated region of tissue between the fossa ovalis and the coronary sinus in continuation with the insertion point of the EV.

The tip of the left atrial appendage LAA contributes to the left side of the cardiac silhouette in a PA image. The LA is a smoother structure with the muscular appendage confined to a small tube-like structure arising from the superior and left side of the chamber. The left sided pulmonary veins are best seen in the LAO projection and are pos- terior to the left atrial appendage.

The right pulmonary veins are best visualized in an RAO projection. The right superior pulmonary vein is posterior to the junction between the right atrium and superior vena cava. The LA myocardial fibers extend over variable distances into the pulmonary veins. These connections are generally the targets for pulmonary vein isolation. The LA wall is generally a thin structure and therefore care must be taken when manipulating catheters in this region. The lateral wall is approximately 3.

This is seen from a posterior view. An ablation catheter is posi- tioned via the intra-atrial septum at the location of the fossa ovalis. The LA is anterior to the esophagus. This is of real importance in terms of pos- terior wall ablation. The esophagus has a variable course in relation to the LA.

There is also a variability in the thickness of the fibrofatty tissue between the LA and the esophagus. In clinical practice this generally results in the application of lower power 25—30 W and shorter duration lesion in the posterior left atrial wall in order to attempt to minimize the possibility of esophageal injury.

Anterior to the LA is the ascending aorta which is an important consideration when performing trans septal access. Atrio-Ventricular AV Junction The compact AV node is the atrial component of the specialized AV junctional area and is located between the coronary sinus os and the septal leaflet of the tricuspid valve. It therefore lies inside the triangle of Koch. It measures approximately 5 mm in length and is histologically quite complex.

It is not insulated by connective tissue and therefore may potentially be damaged by RF application. The inferior extensions of the compact AV node also run within the triangle of Koch with the rightward extension fast pathway parallel to the tricuspid valve and the leftward extension slow pathway towards the coronary sinus.

These extensions pass either side of the AV nodal artery and also are not protected struc- tures. The boundaries of the triangle of Koch are shown superimposed on an anatomic specimen in Fig. This is formed by the coronary sinus CS , septal leaflet of the tricuspid valve TV inferiorly and the tendon of Todaro anterosuperiorly. It is better insulated than the AV node and therefore is not as easily damaged with RF, although this is still pos- sible.

The proximal bundle runs from the distal AV node into the fibrous tissue of the central body where it is termed the penetrating portion. Following this it emerges on the ventricular side of the fibrous body, sandwiched between the membranous septum and the muscular ventricular septum, Taking an initial course usually to the left side of the septum, it then bifurcates into the right bundle RB and left bundle LB branches, still insulated by fibrous tissue sheaths.

The RB tends to have a more anterior origin in the membranous septum. It is approximately 7 cm in length [22] and 6—16 mm in diameter [23]. The coronary sinus is generally surrounded by myocardial musculature which extends from the right and left atrial walls [24].

This musculature may extend for a further 2—11 mm along the great cardiac vein [25]. Distal to this the venous wall is not surrounded by musculature and therefore perforation through instrumentation is more likely. The Valve of Vieussens rarely causes a significant obstruction to the advance- ment of a catheter but rather the acute bend in the vein beyond this or an advance- ment into a side branch are more common causes of cannulation problems. It is therefore better to slowly withdraw and rotate the catheter rather than to try to advance further.

The anterior interventricular vein courses from close to the LV apex and then continues into the great cardiac vein that into the left AV groove under the left atrial appendage [26]. Distally the great cardiac vein receives left atrial veins including the Vein of Marshall and more proximally ventricular veins from the anterior RV and LV and the interventricular septum.

The middle cardiac vein joins the CS close to the os. Occasionally it may also enter the RA directly. This vein runs along the diaphragmatic surface between the LV and RV with a close proximity to the right coronary artery and in particular the branch to the AV node. It may be used to map accessory pathways in the pyramidal space. Given that there are often more than two fascicles the term hemiblock is gener- ally not accurate and fascicular block seems more appropriate.

The QRS is not broad. Posterior fascicular block is less common due to the short and wide nature of this fascicle. Diagrammatic representation of both anterior and posterior fascicular bock are shown in Fig.

This may be due to the multiple ventricular connections of this fascicle mak- ing complete block of this fascicle less likely [27]. There is a variability in the ECG appearances. In general the changes noted are Q waves in V1 and V2 as a result of anteriorly directly right ventricular depolarization [28].

This may also cause a qrS in V1 and V2. There is also loss of q waves in leads V5, V6 and I due to loss or reversal of left to right ventricular septal activation. The QRS is not significantly broad because activation of the left ventricular free wall and apex occurs via the anterosuperior and posteroinferior fascicles. Complete bundle branch block occurs as a result of either partial or complete structural or functional block in one of the two bundle branches resulting in a wid- ening of the QRS greater than ms as well as a change in morphology, which generally reflects conduction down the contralateral bundle with secondary repolarisation.

Following this depolarisation spreads from the apex to the base and to the RV free wall and apex. During this process, septal activation is the pre- dominant force and therefore the vector is anterior and to the left, resulting in a wide slurred QRS in I, aVL and V6 Fig. Depolarization then occurs in a leftward and posterior direction through the LV. Finally, the anterior wall of the LV is depolarized.

The RB branch is an insulated bundle of specialized myocytes that runs as a direct continuation of the atrioven- tricular conduction bundle distal to origin of the left bundle branch. The QRS duration is within normal range with a leftward axis. There is poor R wave progression V1—V3. There is also a tall R wave in lead aVL.

The QRS axis is in a rightward direction. There is an rS in lead aVL. Continuing toward the apex, it divides into several branches one of which courses through the moderator band to the base of the anterior papillary muscle, and then the right ven- tricular free wall. It gives off septal branches which activate the septum almost immediately after left ventricular activation.

Septal activation is generally complete within 35 ms and terminates in Purkinje fibres at the apex. Following this, right ventricular free wall and septal depolarization results in S waves in these leads. The R or r deflection is usually wider than the initial R wave. ST segment deviation is generally discor- dant to the QRS vector. There are four types of aberrancy: The longer RR interval results in a prolonged action potential in the His and bundle branches.

The right bundle usually has a longer action potential duration than the left bun- dle and therefore the following beat with the shorter RR interval is blocked in the right bundle, which is still refractory and conducts down the left bundle with a RBBB morphology Fig. Acceleration dependent This occurs with very slight acceleration of the heart rate less than 5 ms at a critical cycle length which is often within normal heart rate ranges. Of note as the rate increases further, the aberrancy often resolves as the action potential duration of the bundles reduces more than that of the AV node.

Additionally the action potential duration of the bundle branches often reduces in a time dependent manner known as restitution.

Deceleration dependent This occurs following a long pause during which a premature atrial beat conducts to the ventricle with a resultant bundle branch block pattern Fig. A premature atrial complex PAC conducts through the His and conducts along the LB with block in the RB occurs as a result of slow phase IV depolarization of the bundle branches result- ing in refractoriness of one of the bundles as the atrial beat results in depolariza- tion.

The His catheter is positioned so that the proximal electrogram is recording a His deflection and the distal recording is recording a right bundle potential.. The first beat shows a His potential on the proximal electrogram and a right bundle potential on the distal electrogram followed by ventricular activa- tion. The following beat shows a His potential on the proximal electrogram with no right bundle potential on the distal electrogram and a characteristic RBBB pattern on the surface ECG.

Concealed retrograde conduction This occurs when retrograde conduction in one of the bundle branches from a PVC results in refractoriness for the next antegrade beat. As the bundle recovers the next beat which conducts down the contralateral bundle conducts retro- gradely up the bundle again Fig. This continues until a different PVC alters the activation retrograde activation of the bundle. This is a relatively com- mon cause of aberrancy during SVT.

Any number of leads can be recorded in order to electrically visual- ize the heart from different angles. RV a is positioned in the RV apex Fig. These beats then conduct retrogradely X up the RB which is no LB longer refractory RB The standard 12 lead ECG is composed of six unipolar precordial leads posi- tioned as follows across the anterior chest wall: This is a theoretical point close to zero poten- tial created from the electrodes between the right arm, left arm and left leg Fig.

These vectors create three bipolar leads I right arm to left arm , II right arm to left leg and III left arm to left leg through three large resistors.

The electri- cal activation between these three leads therefore cancels out to come close to a zero potential WCT. GCT is created from two of the three Fig. The right leg lead is used to introduce a current to the patient in order to maintain a voltage equivalent to that of the amplifier. This feeds back an inverse of potential low frequency interference and which increases if this lead is disconnected.

The QRS axis refers to the mean direction of ventricular activation in the frontal plane. In theory, the overall direction of electrical activation should be perpendicular to this. As there are two potential perpendicular directions, the leads either side of the isoelectric lead need to be examined and the axis is in the direction of the more positive lead.

In general principles the QRS axis shifts for several reasons. If there is chamber hypertrophy the QRS axis will shift in the direction of the hypertrophied ventricle as there is a greater component of electrical activation in that direction.

In bundle branch block, activation moves from the opposite side to the side with the bundle branch block and therefore the axis will be in the same direction. In cases of myocardial infarc- tion, the axis tends to move in the opposite direction away from the infarcted tissue. Autonomic Innervation of the Heart There is a continual balance between the two main components of the autonomic nervous system; the sympathetic adrenergic and parasympathetic vagal innervation.

The sympathetic efferent neurons innervate the SN as well as the atria, AV node and ventricles acting principally on the beta-adrenoceptors.

The initial rise in intrathoracic pressure results in a elevation in blood pressure Phase I with a stable and then compensatory drop in heart rate.

As well as an elevation in aortic pressure there is a reduction in preload which results in a drop in blood pressure with a rise in heart rate Phase II. As the actual maneuver ends pressure on the aorta is reduced and the blood pressure transiently decreases with a resulting increase in the heart rate Phase III. As the cardiac output increases to normal the blood pressure then increases with a compensatory drop in heart rate Phase IV activity results in positive inotropy, positive chronotropy and an increased conduc- tion velocity.

The parasympathetic vagus nervous system synapses with ganglia acting on muscarinic receptors in the heart. In general the right vagus innervates the SA node while the left vagus innervates the AV node.

The vagus nerve innervates the atria to a lesser extent. There is minimal innervation of the ventricles. Increased vagal stim- ulation results in negative chronotopy and reduced conduction velocity. Given the lack of vagal innervation in the ventricles there is minimal inotropy. There are several methods of assessing autonomic activity of the heart including the valsalva maneuver and the tilt table test.

The valsalva maneuver is performed by exhaling with a closed glottis for a period of 10 s therefore increasing intrathoracic pressure.

There are four phases as depicted in Fig. Phase I: Transient increase in blood pressure with no change in heart rate as a result of compression of the ventricles and aorta. Phase II: A significant reduction or plateau in blood pressure as a result of com- pression of the intrathoracic vena cava reducing venous return. Phase III: As the maneuver has now stopped the intrathoracic pressure returns to normal reversing phase I and resulting in a reduction in left ventricular output and an increase in right ventricular output as a result of an increase in venous return.

Phase IV: As the venous return increases further there is an increase in the cardiac output and blood pressure.

Clinical Cardiac Electrophysiology: Techniques and Interpretations.

This results in stimulation of baroreflex which increases parasympathetic activity resulting in a reduction in heart rate. A tilt table test may be useful in patients with a history of pre-syncope, syncope or postural symptoms such as palpitations when structural heart disease has been excluded.

During this test the patient is attached to a specialized table and posi- tioned at a 60—70 degree angle. The ECG and non-invasive blood pressure are con- tinually monitored. Although some laboratories do not gain an intravenous IV due to the potential effects on vagal tone, it is reasonable to insert an IV for the admin- istration of pharmacological agents and wait for 15 min prior to commencing the test.

The patient is monitored in the supine position for five minutes and then placed in an upright position at a 60—70 degree angle. The heart rate and blood pressure are monitored and recorded every five minutes for 45 min.

If there is an acute drop in blood pressure or loss of consciousness, the table is returned to the supine position. It is not uncommon to get a slight drop in blood pressure with isoprenolol and therefore this test is generally only considered positive if syncope occurs.

Carotid sinus massage can often be per- formed either in the supine or erect position, the latter having a slightly higher yield. If there is associated syncope then this is defined as carotid sinus syn- drome. Carotid sinus hypersensitivity is more common in the elderly and in males, and is extremely uncommon in individuals under the age of 40 years.

Carotid sinus massage should not be performed in patients with a prior transient ischemic attack or stroke within the prior three months, or in patients with a carotid artery bruit unless significant carotid artery disease has been excluded on carotid dopplers. Both nitrates and isoprenolol increase the sensitivity but reduce the specificity of the tilt table test.

If syncope occurs in association with bradycardia or reflex hypotension the diag- nosis is neurocardiogenic syncope. If the major precipitant is bradycardia this is cardio-inhibitory, and if the major precipitant is hypotension it is vasodepressor.

Other potential causes such as medications or prolonged bed rest which may alter vascular tone should be excluded prior to making this diagnosis. POTS can be divided into either partial dysautonomic or hyperadrenergic types.

In partial dysautonomic POTS the increase in heart rate is partially due to increased blood pooling in the lower limbs as a result of an alteration in the con- trol of vascular tone. In hyperadrenergic POTS there is often an associated increase in blood pressure associated with the increase in heart rate.

The tilt table results depend on the age of the patient, with younger patients more likely to have cardioinhibitory neuro- cardiogenic syncope, and older patients more likely to have vasodepressor neurocardiogenic syncope. Important Points to Remember 1. The cardiac action potential is composed of 4 phases. In both the SN and AV nodes there is a slow spontaneous diastolic depolarization which merges with Phase 0 resulting in spontaneous automaticity while Phase IV in other cells is generally more flat.

Phase 0 rapid depolarization occurs when the membrane potential becomes positive. It is much more prominent in the purkinje and epicardial cells. Phase II plateau phase occurs when the action potential becomes rela- tively flat and does not occur in the SN or AV node. Phase III rapid repolarization occurs when there is restoration of the membrane potential to the resting phase.

Refractoriness describes the period during which a stimulus does not result in a new depolarization after phase 0 of the cardiac action potential. The absolute RP is the longest coupling interval which does not result in local capture. Re-Entry occurs when a wave of excitation moves around a circuit which is determined anatomically, functionally or a combination of the two.

There must be two or more pathways for conduction Unidirectional block in one pathway Alternative conduction over the other pathway with sufficient delay as to retrogradely invade the formerly blocked pathway 4. Automaticity results from spontaneous depolarization during phase IV of the action potential. Afterdepolarizations are defined as depolarizations which occur after Phase 0 of the cardiac action potential and may result in a spontaneous action potential known as a triggered response.

DADs occur as a result of an increase in the inward movement of cal- cium. The RAO projection helps to demonstrate the postero-anterior PA loca- tion of a catheter within the cardiac chambers and shows the AV groove more clearly than the PA view.

Following discharge from the SN conduction occurs through the RA pre- dominantly utilizing aligned myocytes. AV conduction occurs through the AV junctional region, the atrial com- ponent of which is termed the AV node. This is located between the coro- nary sinus os and the septal leaflet of the tricuspid valve. The His bundle is a continuation of the compact AV node. Although it has similar cellular components it is better insulated than the AV node and therefore is not as easily damaged with RF.

The proximal bundle runs from the distal AV node to the fibrous tissue of the central body where it is termed the penetrating portion. Following this it bifurcates into the right bundle RB and left bundle LB branches at the level of the septal TV leaflet.

The RB tends to have a more anterior origin than the LB. The LB branch originates below the right and non-coronary cusps and then courses along the LV septal surface. During this process, septal activation is the pre- dominant force and therefore the vector is anterior and to the left, resulting in a wide slurred QRS in I, aVL and V6.

Depolarization then occurs in a leftward and pos- terior direction through the LV. Septal fascicular block has a variable ECG appearances. In general the changes noted are Q waves in V1 and V2 as a result of anteriorly directly right ventricular depolarization.

The RB branch is an insulated bundle of fibers as a direct continuation of the penetrating atrioventricular bundle. It runs along the RV septum to the apex where it becomes subendocardial in the mid septum running along the posterior margin of the septal band, courses through the moderator band to the base of the anterior papillary muscle, and then the right ven- tricular free wall.

ST segment deviation is generally discordant to the QRS vector. The right bundle has a longer AP duration than the left bundle and therefore the following beat with the shorter RR interval is blocked in the right bundle which is still refractory and conducts down the left bundle with a RBBB morphology. Acceleration dependent aberrancy occurs with very slight acceleration of the heart rate less than 5 ms at a critical cycle length which is often within normal heart rate ranges.

This tends to occur more commonly in the left bundle resulting in LBBB. Deceleration dependent aberrancy occurs following a long pause during which a premature atrial beat conducts to the ventricle with a resultant bundle branch block. Aberrancy due to concealed retrograde conduction occurs when retro- grade conduction in one of the bundle branches from a PVC results in refractoriness for the next antegrade beat. As the bundle recovers the next beat which conducts down the contralateral bundle conducts retrogradely up the bundle again.

References 1. Dhamoon AS, Jalife J. The inward rectifier current IK1 controls cardiac excitability and is involved in arrhythmogenesis. Heart Rhythm. Antzelevitch C, Burashnikov A, et al. Overview of basic mechanisms of cardiac arrhythmia. Card Electrophysiol Clin. Anatomic variations of the orifice of the human coronary sinus. Opthof T. The mammalian sinoatrial node. Cardiovasc Drugs Ther.

The sinoatrial node, a heterogeneous pacemaker structure. Cardiovasc Res. DiFrancesco D, Ojeda C. Properties of the current if in the sino-atrial node of the rabbit com- pared with those of the current IK2, in Purkinje fibres. J Physiol. DiFrancesco D. The role of the funny current in pacemaker activity. Circ Res.

DiFrancesco D, Tortora P.

Josephson - Clinical Cardiac Electrophysiology Techniques An

Direct activation of cardiac pacemaker channels by intracellular cyclic AMP. DiFrancesco D, Tromba C. Muscarinic control of the hyperpolarization-activated current If in rabbit sino-atrial node myocytes.

Am J Physiol. Olshansky B, Sullivan RM. Inappropriate sinus tachycardia. J Am Coll Cardiol. Clinical efficacy of ivabradine in patients with inap- propriate sinus tachycardia: Radiofrequency catheter ablation of inappropriate sinus tachycardia guided by activation mapping.

The terminal crest: The importance of atrial structure and fibers. Clin Anat. Atrial structures and fibers: The inferior right atrial isthmus: J Cardiovasc Electrophysiol. James TN. The connecting pathways between the sinus node and the A—V node and the A—V node and the right and left atrium in the human heart.

Am Heart J. James TN, Sherf L. Specialized tissues and preferential conduction in the atria of the heart. Am J Cardiol. Anatomy of the left atrium: Inoue S, Becker AE.

Posterior extensions of the human compact atrioventricular node: Anatomy of cardiac nodes and atrioventricular specialized con- duction system. Rev Esp Cardiol. Major coronary sinus abnormalities identification of occurrence and significance in radiofrequency ablation of supraventricular tachycardia. Tschabitscher M. Anatomy of coronary veins the coronary sinus. Proceedings of the 1st international symposium on Myocardial Protection via the Coronary Sinus. Steinkopff Verlag; The anatomic basis of connections between the coronary sinus musculature and the left atrium in humans.

Myocardial coverage of the coronary sinus and related veins. A review of the coronary venous system: Nakaya Y, Hiraga T. Reassessment of the subdivision block of the left bundle branch. Jpn Circ J. Postural tachycardia, orthostatic intolerance and the chronic fatigue syndrome. Grubb BP, Olshansky B, editors.

Read Josephson's Clinical Cardiac Electrophysiology Ebook Online

Significant developments in the understanding of arrhythmias as well as technologi- cal advances have allowed electrophysiology studies to be considered as a diagnos- tic first line option. This chapter discusses the fundamental principles of invasive electrophysiology and provides an essential guide in terms of establishing the cor- rect diagnosis and ablation strategy. Indications for an EP Study and Ablation The overall decision on whether to perform an EP study and ablation depends on the balance between the potential benefits, alternative treatment options, risks as well as the individual patient preference.

In general for symptomatic supraventricular B. The decision for the invasive management of AF and VT is often more complex and requires very careful examination of the patients symptoms and potential complica- tions which must be balanced against alternative treatment options. As techniques and technology improve for more complex ablations the threshold for an invasive strategy is already clearly changing. Although it is ideal to have inducible tachycardia at the start of the EP study this is not critical and it is entirely reasonable to perform an ablation if either dual AV nodal anatomy or accessory pathway conduction is present in the setting of electrocardiographic evidence of an SVT.

The issue of ablation in the setting of asymptomatic ventricular pre-excitation is somewhat more complex. Ablation is indicated in patients with high-risk occupa- tions such as pilots, scuba divers and school bus drivers [1]. Inducibility of AVRT in the absence of symptoms may be considered as an indication for ablation although this is not a clear cut decision and may also depend on patient and physi- cian preference as well as the conduction properties of the pathway. Accessory pathways that can lead to rapid ventricular rates during atrial fibrillation should be ablated.

Atrial pacing may be used to calculate the antegrade refractory period of the AP with a measurement greater than ms being considered lower risk. These measurements may help to guide the decision regarding ablation of an AP. Typical Atrial Flutter Typical atrial flutter involving the cavo-tricuspid isthmus CTI can be successfully ablated in the majority of cases.

Ablation can also be considered for atypical atrial flutter Class IIa Indication; Level of Evidence B although the overall success may not be as high as for typical atrial flutter [1] Fig.

This is extremely important as symptoms may be non-specific and therefore it is often useful to consider an electrical cardio- version and reassess after sinus rhythm has been established. Additionally all patients who are being considered for a catheter ablation must be able to tolerate anticoagulation therapy at least during and after their ablation [2].

There is insuffi- cient data to support routine withdrawal of oral anticoagulation following an AF ablation even if it appears successful and the longer term decision regarding oral anticoagulation should be based on the CHADS2VASC score [2]. This is because patients may continue to have asymptomatic episodes of AF which continue to pose a thrombo-embolic risk. Catheter ablation can also be considered for the management of longstanding persistent symptomatic AF Class IIb Indication, Level of Evidence B although the overall success for such a procedure may not be high.

If available in the center, a hybrid ablation with thora- coscopic approach and closure of the left atrial appendage offers a better future in these patients [3] Fig. AAD anti- arrhythmic drug therapy Ventricular Arrhythmias Catheter ablation is recommended for patients with sustained monomorphic VT including VT terminated by an ICD where anti arrhythmic drug therapy is either ineffective or not tolerated as well as the control of incessant VT [4]. It may also be considered when anti-arrhythmic drug therapy has not failed and in particular may be a suitable alternative to amiodarone therapy.

EP Study and Ablation: Patient Preparation The most useful test for any patient prior to an EP Study is an ECG or rhythm strip of the arrhythmia as this may guide the entire approach, chamber of access and threshold for potential ablation. A baseline ECG should be performed as well as electrolytes and urea, full blood count and an international normalized ratio for patients taking warfarin [5]. For potentially high risk procedures a group and crossmatch should be considered.

In general for most diagnostic studies anti-arrhythmic drugs should be stopped for at least 5 half lives. This is not required in patients undergoing catheter ablation unless an EP study or rotor mapping is also being performed. Potential Risks The risks associated with EP studies and ablation vary greatly depending on the procedure being performed.

General complications include groin hematoma, vascu- lar injury and pericardial effusion. More specific complications may occur in AF and VT ablations. In general many of these risks can be significantly minimized if care is taken and appropriate action taken. These risks, as well as preventative mea- sures are summarized on Table 2. Table 2. VTs 0. It is therefore important to be gentle with all of the equipment being used.

Some regions within the heart are particularly thin and extra caution should be taken. As demonstrated in Fig. The incidence of perfora- tion resulting in either a pericardial effusion or tamponade is 1. For SVT ablations this is 0. Accumulation may also be localized and therefore may occur on the left side prior to the right side. The accumulation of a significant pericardial effusion may be associated with an increase in heart rate with or preceding a drop in blood pressure. It must also be noted, however, that an increase in sympathetic drive may initially result in an increase in the blood pressure.

Pericardial stretch may occasionally result in an increase in parasympathetic tone with a transient bradycardia and hypotension. A drop in blood pressure is a relatively late sign of acute pericardial effusion and it is therefore important to monitor for earlier signs. A reduction in the left lateral wall excursion in the LAO fluoroscopic view has been shown to be associated with pericardial effusion [21]. This occurs as the peri- cardium is relatively fixed to the spine and the sternum and therefore fluid in the pericardial space is more likely to accumulate posterolaterally followed by antero- laterally.

The accu- mulation of a small pericardial effusion detected on ICE during an AF ablation may indicate an increase in the risk of a late post procedure pericardial effusion while no evidence of effusion on ICE indicates a very low post procedural risk. All EP laboratories should have equipment for emergency pericardiocentesis including rapid access to echocardiography. In order to keep this as simple as possible the needle used to access the femoral vein and a 0.

After confirmation that the wire is within the pericardial space by pushing it as far as possible and ensuring that it is not within one or more cardiac chambers a short sheath and a pigtail catheter can be used to rapidly drain the effusion. Phrenic Nerve Injury The right phrenic nerve runs alongside the SVC and passes laterally along the RA running anteriorly to the right pulmonary veins passing more closely to the superior than the inferior right pulmonary vein Fig.

The left phrenic nerve runs over the fibrous pericardium with a variable course over the LA and LV and terminates in the left hemidiaphragm. The incidence of phrenic nerve palsy following an AF ablation is approximately 0. This generally occurs with isolation of the right superior pulmonary vein or the superior vena cava. Left phrenic nerve palsy is less common but may occur in left atrial appendage ablation. Various techniques may be used to help map the location of the phrenic nerve before or during catheter ablation.

Pacing at high output may be performed in order to assess for phrenic nerve capture. The vagus nerve is also seen in both images prior to performing this maneuver as muscle relaxants are often administered which will inhibit the effects of pacing on the phrenic nerve.

Additionally the diaphragm can be monitored using fluoroscopy during ablation in the absence of nerve para- lytic agents. More novel techniques such as recording electromyograms from the diaphragm have been described in which either a catheter is positioned in the hepatic vein or modified surface electrodes are positioned over the diaphragm with pacing performed from either subclavian vein. Phrenic nerve palsy is generally noted on CXR as an elevated hemidiaphragm and may be associated with dyspnea, a cough or hiccups.

The majority of phrenic nerve palsy recovery within 9 months. In this lateral image the ascending aorta Ao is anterior to the left atrium LA. The oesophagus Oe is posterior to the left atrial wall.

Also seen in this image is the descending aorta DAo posterior wall of the LA and the anterior portion of the esophagus is variable but may be as little as 5 mm [23]. The location of the esophagus may run either central to the posterior wall of the left atrium, towards the left pulmonary veins or towards the right pulmonary veins as is generally closer at the atrial pulmonary vein junction and in more inferior locations.

Although the esophagus can be clearly visualized on a pre-ablation CT scan the esophagus is a mobile structure and therefore the loca- tion may change during the procedure. Esophageal injury occurs predominantly as a result of direct thermal injury from catheter ablation along the posterior wall of the LA. Other contributing factors may include damage to the arterial flow to the esophagus as well as to the vagus nerve and plexus.

This may result in mucosal erythema, esophagitis or atrioesophageal fistula. Discrete mucosal changes have been noted to be present in approximately half of all patients who undergo catheter ablation for AF with almost one fifth devel- oping esophageal ulceration [24].

The incidence of fistula formation between the left atrium and the esophagus as a result of catheter ablation for AF ranges from 0.

Symptoms relating to atrio-esophageal fistula may occur from 3 days to 6 weeks post ablation and are often non specific. The most common is a pyrexia fol- lowed by neurological symptoms relating to thrombo-embolism.

Other symptoms include chest pain and dysphagia. The white cell count is generally elevated. Management depends on acute recognition of the condition followed by surgical repair. Although the esophagus can be visualized pre-procedure this is generally unreli- able due to intra-procedural movement.

The esophagus can be visualized during ablation using fluoroscopy with a marker such as a naso-gastric tube, a temperature probe or barium paste. Esophageal temperature monitoring is performed by some operators using a tem- perature probe. Evidence for the efficacy in preventing esophageal injury is limited and conflicting and overall there is no general consensus as to whether luminal esophageal temperature is a good predictor of mucosal injury.

It is generally considered reasonable to limit maximum power to 25—30 W and to spend no longer than 30 s on one region when ablating along the posterior wall of the left atrium. It is also common to prescrive proton pump inhibitors post ablation in order to reduce the effects of acid reflux on the esophagus. Coronary Artery Injury This may occur if ablation is performed in close proximity to a coronary artery such as the aortic cusps. Other regions where ablation may be in close proximity to a coronary artery or one of its branches include the coronary sinus as shown in Fig.

Endocardial ablation of accessory pathways along the mitral and tricuspid annu- lus carries a low risk of coronary artery stenosis. The posterolateral branch of the RCA or the circumflex coronary artery often run closely to this location and this may be a closer to the anterior and inferior walls of the Fig. The RCA originates in the right coronary cusp of the aortic root and courses along the right atrioventricular grove anteriorly and inferiorly where it eventually courses towards the proximal coronary sinus CS.

In this region there is close proximity to the CS. If ablation is being performed in this location a coronary angiogram should be considered and a minimum distance of 5 mm should be maintained between the site of ablation and the coronary artery. Epicardial ablation is now increasingly performed particularly for non-ischemic VT and to a lesser degree ischemic VT. Coronary CT or angiography should be performed in these cases prior to ablation. One gray is defined as the absorp- tion of 1 J of ionizing radiation by 1 Kg of matter.

The equivalent dose Sievert is the absorbed dose in Gy multiplied by the radiation weighting factor which varies according to the source of radiation and is 1 for X-rays.

This can be further modi- fied in order to calculate the effective dose when the radiation is predominantly exposed to certain regions of the body. This can be achieved by reducing the frame rate to as low as possible, minimizing the duration of time performing fluo- roscopy and not taking cine images. The development of 3 D mapping systems has had a significant impact on reducing the need for fluoroscopy particularly in com- plex ablations.

Administration of Sedation and Anesthesia The requirements for sedation and anesthesia vary according to the precise proce- dure being performed. For EP studies minimal doses of sedation are given for anx- iolytic effects as larger doses may reduce the inducibility of the arrhythmia particularly in adrenaline sensitive focal atrial tachycardia and outflow tract tachy- cardia. Moderate doses of sedation are often required for ablation and in particular for performing anatomical lesions such as a cavotricuspid isthmus ablation.

Ablation for AF and complex VT may be performed with moderate to deep sedation or gen- eral anesthesia. There are several potential advantages to the use of general anesthe- sia in such procedures such as minimizing patient discomfort and movement thus facilitating 3D mapping as well as allowing the use of TEE visualization.

Care must be taken in order to minimize the doses of paralytic agents when assessing for phrenic nerve capture. Benzodiazepines and opioids are used in the EP laboratory for their anxiolytic and partial amnesic effects.

All patients undergoing any procedure involving the administra- tion of intravenous sedation should have a history and rapid airway assessment prior to starting the procedure. Ideally there should be involvement of an anes- thesiologist.

All patients should be closely monitored post procedure until their vital parameters have returned to normal limits. The most common benzodiazepines used in the EP laboratory are midazolam and diazepam. Although either of these agents can be used midazolam tends to have a shorter duration of action particularly in the elderly or in those with reduced car- diac output, respiratory depression, hepatic and renal impairment. Midazolam can be administered at a dose of 0.

Generally no more than 10 mg is needed for the entire procedure. Midazolam tends to have less effect on suppression of induction of supraven- tricular tachycardia compared to diazepam. Routine administration of the benzodi- azepine antagonist flumazenil should not be performed and this should be reserved only for cases of significant over sedation.

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A dose of 0. The patient should be monitored closely for 2 h in order to ensure that there are no further sedative effects as the drug effects wear off. Fentanyl is a useful opioid which can be administered at the start of the case at a dose of 0.

The overall duration of action is approxi- mately 30—60 min. If used in conjunction with a benzodiazepine fentanyl may result in respiratory depression and therefore monitoring is required. The effects of fentanyl can be partially reversed by naloxone at a dose of 0. Propofol is frequently used in the EP laboratory. The individual responsibility for this depends on the country where the procedure is performed. Propofol is gen- erally administered at a dose of 0. Further doses may be administered in 5 mg boluses if required.

It has no significant electrophysi- ological effects on arrhythmia induction. Very occasionally propofol infusion syndrome may occur particularly at higher doses and for longer periods of time. This may occur as a result of mito- chondrial respiratory chain inhibition or impaired fatty acid metabolism and results in acute refractory bradycardia leading to asystole with either metabolic acidosis, rhabdomyolysis, hyperlipidaemia, and or fatty liver.

The only effective treatment for this condition is haemodialysis or haemoperfusion with cardiorespiratory support. Peri-procedural Anticoagulation For the majority of right sided ablations anticoagulation is not required although some operators choose to give low dose heparin in order to try to lower the potential risk of deep venous thrombosis and pulmonary embolism.

For left sided ablations intravenous heparin is administered aiming for an Activated Clotting Time ACT of greater than s. In patients who are already taking oral anticoagulation the decision to continue, discontinue or bridge with heparin depends on the risks of thrombo-embolism compared to the risk of bleeding.

If this is 0 then anticoagulation is generally not required pre-ablation however in all other cases therapeutic anticoagu- lation is recommended for a minimum period of 4 weeks [2] Table 2. This occurs as a result of endothelial injury as well as potential mechanical dysfunction of the left atrium post ablation.

It is therefore necessary to administer heparin for left sided ablations aiming for an activated clotting time ACT of s [2] even in patients who are receiving warfa- rin. In patients who are allergic to heparin bivalirudin may be considered. It is recommended that oral anticoagulation is continued for at least 8 weeks post ablation in these patients and long-term in patients with a higher risk of thromboem- bolism [2].

The choice of whether to continue with oral anticoagulation compared with heparin bridging is largely dependent on individual operator and center experi- ence. Continuation of warfarin during catheter ablation for AF is likely superior to bridging with heparin with reported lower rates of thrombo-embolism, pericar- dial effusion and major bleeding [27]. Although there is limited data regarding the use of uninterrupted direct oral anticoagulants in AF catheter ablation given the shorter half life of the direct oral anticoagulants minimal interruption can be performed pre-ablation and appears to be effective particularly if a pre-procedure Table 2.

In general provided the patient has normal renal function the last dose of oral anticoagulant can be admin- istered 24 h pre ablation with the first dose post procedure administered 4 h after sheath removal. EP Laboratory Set-Up The EP lab is composed of an EP recording system, a stimulator, a RF generator with the potential for irrigation and an electroanatomic mapping EAM system as well as a cryoablation system and the cables and interfaces which connect these systems.

Additional to this is resuscitation at least one defibrillator with rapid access to a second and ventilation equipment and fluoroscopic equipment for image acquisition Fig. Amplification and Filtering Electrograms recorded in the heart are generally less than 5 mV in amplitude and often as small as 0. In order to display these signals they must be amplified and filtered. Signals may be amplified up to 10, times prior to being filtered.

The amplified signal then passes through a high pass filter. This allows higher frequency signals to pass through while removing signals below a designated fre- quency. On the surface ECG this is set very low at 0. For bipolar intracardiac signals this is set higher at 30 Hz which therefore filters out a larger range of low frequen- cies that may occur as a result of catheter movement, electrical farfield or respira- tory variability.

For unipolar intracardiac signals where the morphology of the signal is more relevant the setting is similar to the surface ECG at 0. This signal then passes through an isolation amplifier which isolates the current from the patient and is subsequently transmitted through a low pass filter. This is generally set at Hz for bipolar intracardiac electrograms and filtered and unfiltered unipolar electrograms and Hz for surface ECG sig- nals Fig. Additionally most EP systems have a notch filter, which removes signals at a specific frequency range generally in the range of electrical frequency.

This is often set at 50 Hz in Europe and 60 Hz in North America and is designed to reject interference outside of the range around this. This also has several potential disadvantages including a reduction in the amplitude of certain electrograms such as pulmonary vein potentials as well as the potential to add interference.

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